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Gene expressions and roles of matrix metalloproteinases-8 and tissue inhibitor of metalloproteinases-1 in hyperoxia-induced pulmonary fibrosis in neonatal rats.
Zhongguo Dang Dai Er Ke Za Zhi. 2007 Feb; 9(1):1-5.ZD

Abstract

OBJECTIVE

Extracellular matrix (ECM) deposition is a major reason of pulmonary fibrosis in hyperoxia-induced lung injury. However, the relevant mechanism has not been identified. This study examined the gene expressions of matrix metalloproteinases-8 (MMP-8, a catabolic enzyme of type I collagen) and tissue inhibitor of metalloproteinases-1 (TIMP-1) in neonatal rats with hyperoxia-induced pulmonary injury in order to explore the role of MMP-8 and TIMP-1 in pulmonary fibrosis.

METHODS

Eighty term newborn rats were randomly exposed to hyperoxia (FiO2=0.90, hyperoxia group)and to room air (FiO2=0.21, control group)(n=40 each). Lung injury was induced by hyperoxia exposure. The content of type I collagen and the expressions of type I collagen protein and MMP-1 mRNA and TIMP-1 mRNA were assayed with enzyme linked immunoadsorbent (ELISA), immunohistochemistry and reverse transcription polymerase chain reaction (RT-PCR) respectively on days 1, 3, 7, 14 and 21 after exposure.

RESULTS

The content of type I collagen and the expression of type I collagen protein in the hyperoxia group were statistically higher than those in the control group at 14 and 21 days post-exposure. The MMP-8 mRNA expression decreased while the TIMP-1 mRNA expression increased significantly in the hyperoxia group as compared to the control group at 14 and 21 days post-exposure.

CONCLUSIONS

Hyperoxia exposure down-regulates MMP-8 mRNA expression and up-regulates TIMP-1 mRNA expression. This results in a reduction of ECM degradation, thereby ECM deposition occurs in lung tissue, which may be an important mechanism of pulmonary fibrosis following hyperoxia-induced lung injury.

Authors+Show Affiliations

Department of Pediatrics, Second Affiliated Hospital, China Medical University, Shenyang 110004, China.No affiliation info available

Pub Type(s)

Journal Article
Research Support, Non-U.S. Gov't

Language

eng

PubMed ID

17306066

Citation

Fu, Jian-Hua, and Xin-Dong Xue. "Gene Expressions and Roles of Matrix Metalloproteinases-8 and Tissue Inhibitor of Metalloproteinases-1 in Hyperoxia-induced Pulmonary Fibrosis in Neonatal Rats." Zhongguo Dang Dai Er Ke Za Zhi = Chinese Journal of Contemporary Pediatrics, vol. 9, no. 1, 2007, pp. 1-5.
Fu JH, Xue XD. Gene expressions and roles of matrix metalloproteinases-8 and tissue inhibitor of metalloproteinases-1 in hyperoxia-induced pulmonary fibrosis in neonatal rats. Zhongguo Dang Dai Er Ke Za Zhi. 2007;9(1):1-5.
Fu, J. H., & Xue, X. D. (2007). Gene expressions and roles of matrix metalloproteinases-8 and tissue inhibitor of metalloproteinases-1 in hyperoxia-induced pulmonary fibrosis in neonatal rats. Zhongguo Dang Dai Er Ke Za Zhi = Chinese Journal of Contemporary Pediatrics, 9(1), 1-5.
Fu JH, Xue XD. Gene Expressions and Roles of Matrix Metalloproteinases-8 and Tissue Inhibitor of Metalloproteinases-1 in Hyperoxia-induced Pulmonary Fibrosis in Neonatal Rats. Zhongguo Dang Dai Er Ke Za Zhi. 2007;9(1):1-5. PubMed PMID: 17306066.
* Article titles in AMA citation format should be in sentence-case
TY - JOUR T1 - Gene expressions and roles of matrix metalloproteinases-8 and tissue inhibitor of metalloproteinases-1 in hyperoxia-induced pulmonary fibrosis in neonatal rats. AU - Fu,Jian-Hua, AU - Xue,Xin-Dong, PY - 2007/2/20/pubmed PY - 2007/3/21/medline PY - 2007/2/20/entrez SP - 1 EP - 5 JF - Zhongguo dang dai er ke za zhi = Chinese journal of contemporary pediatrics JO - Zhongguo Dang Dai Er Ke Za Zhi VL - 9 IS - 1 N2 - OBJECTIVE: Extracellular matrix (ECM) deposition is a major reason of pulmonary fibrosis in hyperoxia-induced lung injury. However, the relevant mechanism has not been identified. This study examined the gene expressions of matrix metalloproteinases-8 (MMP-8, a catabolic enzyme of type I collagen) and tissue inhibitor of metalloproteinases-1 (TIMP-1) in neonatal rats with hyperoxia-induced pulmonary injury in order to explore the role of MMP-8 and TIMP-1 in pulmonary fibrosis. METHODS: Eighty term newborn rats were randomly exposed to hyperoxia (FiO2=0.90, hyperoxia group)and to room air (FiO2=0.21, control group)(n=40 each). Lung injury was induced by hyperoxia exposure. The content of type I collagen and the expressions of type I collagen protein and MMP-1 mRNA and TIMP-1 mRNA were assayed with enzyme linked immunoadsorbent (ELISA), immunohistochemistry and reverse transcription polymerase chain reaction (RT-PCR) respectively on days 1, 3, 7, 14 and 21 after exposure. RESULTS: The content of type I collagen and the expression of type I collagen protein in the hyperoxia group were statistically higher than those in the control group at 14 and 21 days post-exposure. The MMP-8 mRNA expression decreased while the TIMP-1 mRNA expression increased significantly in the hyperoxia group as compared to the control group at 14 and 21 days post-exposure. CONCLUSIONS: Hyperoxia exposure down-regulates MMP-8 mRNA expression and up-regulates TIMP-1 mRNA expression. This results in a reduction of ECM degradation, thereby ECM deposition occurs in lung tissue, which may be an important mechanism of pulmonary fibrosis following hyperoxia-induced lung injury. SN - 1008-8830 UR - https://www.unboundmedicine.com/medline/citation/17306066/Gene_expressions_and_roles_of_matrix_metalloproteinases_8_and_tissue_inhibitor_of_metalloproteinases_1_in_hyperoxia_induced_pulmonary_fibrosis_in_neonatal_rats_ L2 - https://medlineplus.gov/pulmonaryfibrosis.html DB - PRIME DP - Unbound Medicine ER -